scholarly journals Luxotonic signals in human prefrontal cortex: A possible substrate for effects of light on mood and cognition

2020 ◽  
Author(s):  
Shai Sabbah ◽  
Michael S. Worden ◽  
Daniel Laniado ◽  
Rebeca Waugh ◽  
David M. Berson ◽  
...  

AbstractLight impacts mood and cognition of humans and other animals in ways we are only beginning to recognize. These effects are thought to depend upon a specialized retinal output signal arising from intrinsically photosensitive retinal ganglion cells (ipRGCs) that is being dedicated to a stable representation of the intensity of environmental light. Insights from animal studies now implicate a previously unknown pathway in the effects of environmental light on mood. A subset of ipRGCs transmits light-intensity information to the dorsothalamic perihabenular nucleus, which in turn, innervates the medial prefrontal cortex that plays a key role in mood regulation. While the prefrontal cortex has been implicated in depression and other mood disorders, its ability to encode the level of environmental light (luminance) has never been reported. Here, as a first step to probing for a similar retino-thalamo-frontocortical circuit in humans, we used functional magnetic resonance imaging (fMRI) to identify brain regions in which activity depended on luminance level where activity was modulated either transiently or persistently by light. Twelve brain regions altered their steady-state activity according to luminance level. Most were in the prefrontal cortex or in the classic thalamocortical visual pathway; others were found in the cerebellum, caudate, and pineal. Prefrontal cortex and pineal exhibited reduced BOLD signal in bright light, while the other centers exhibited increased BOLD signals. The light-evoked prefrontal response was affected by light history and closely resembled those of ipRGCs. Although we did not find clear correspondence between the luxotonic regions in humans and those in mice, the persistence and luxotonic nature of light-evoked responses in the human prefrontal cortex may suggest that it receives input from ipRGCs, just like in the mouse. We also found seventeen regions in which activity varied only transiently with luminance level. These regions, which are involved in visual processing, motor control, and cognition, were in the cerebral cortex, diverse subcortical structures, and cerebellum. Therefore, our results demonstrate the effects of light on diverse brain centers that contribute to motor control, cognition, emotion, and reward processing.

2020 ◽  
pp. 287-296
Author(s):  
Daniel C. Javitt

Glutamate theories of schizophrenia were first proposed over 30 years ago and since that time have become increasingly accepted. Theories are supported by the ability of N-methyl-D-aspartate receptor (NMDAR) antagonists such as phencyclidine (PCP) or ketamine to induce symptoms that closely resemble those of schizophrenia. Moreover, NMDAR antagonists uniquely reproduce the level of negative symptoms and cognitive deficits observed in schizophrenia, suggesting that such models may be particularly appropriate to poor outcome forms of the disorder. As opposed to dopamine, which is most prominent within frontostriatal brain regions, glutamate neurons are present throughout cortex and subcortical structures. Thus, NMDAR theories predict widespread disturbances across cortical and thalamic pathways, including sensory brain regions. In auditory cortex, NMDAR play a critical role in the generation of mismatch negativity (MMN), which may therefore serve as a translational marker of NMDAR dysfunction across species. In the visual system, NMDAR play a critical role in function of the magnocellular visual system. Deficits in both auditory and visual processing contribute to social and communication deficits, which, in turn, lead to poor functional outcome. By contrast, NMDAR dysfunction within the frontohippocampal system may contribute to well described deficits in working memory, executive processing and long-term memory formation. Deficits in NMDAR function may be driven by disturbances in presynaptic glutamate release, impaired metabolism of NMDAR modulators such as glycine or D-serine, or intrinsic abnormalities in NMDAR themselves.


2021 ◽  
Vol 15 ◽  
Author(s):  
Emma R. Huels ◽  
Trent Groenhout ◽  
Christopher W. Fields ◽  
Tiecheng Liu ◽  
George A. Mashour ◽  
...  

Studies aimed at investigating brain regions involved in arousal state control have been traditionally limited to subcortical structures. In the current study, we tested the hypothesis that inactivation of prefrontal cortex, but not two subregions within parietal cortex—somatosensory barrel field and medial/lateral parietal association cortex—would suppress arousal, as measured by an increase in anesthetic sensitivity. Male and female Sprague Dawley rats were surgically prepared for recording electroencephalogram and bilateral infusion into prefrontal cortex (N = 13), somatosensory barrel field (N = 10), or medial/lateral parietal association cortex (N = 9). After at least 10 days of post-surgical recovery, 156 μM tetrodotoxin or saline was microinjected into one of the cortical sites. Ninety minutes after injection, rats were anesthetized with 2.5% sevoflurane and the time to loss of righting reflex, a surrogate for loss of consciousness, was measured. Sevoflurane was stopped after 45 min and the time to return of righting reflex, a surrogate for return of consciousness, was measured. Tetrodotoxin-mediated inactivation of all three cortical sites decreased (p < 0.05) the time to loss of righting reflex. By contrast, only inactivation of prefrontal cortex, but not somatosensory barrel field or medial/lateral parietal association cortex, increased (p < 0.001) the time to return of righting reflex. Burst suppression ratio was not altered following inactivation of any of the cortical sites, suggesting that there was no global effect due to pharmacologic lesion. These findings demonstrate that prefrontal cortex plays a causal role in emergence from anesthesia and behavioral arousal.


Author(s):  
James P. Herman

Appropriate control of the HPA (hypothalamo-pituitary-adrenocortical axis) is required for adaptation to physiological and environmental challenges. Inadequate control is linked to numerous stress-related pathologies, including PTSD, highlighting its importance in linking physiological stress responses with behavioral coping strategies. This chapter highlights neurocircuit mechanisms underlying HPA axis adaptation and pathology. Control of the HPA stress response is mediated by the coordinated activity of numerous limbic brain regions, including the prefrontal cortex, hippocampus, and amygdala. In general, hippocampal output inhibits anticipatory HPA axis responses, whereas amygdala subnuclei participate in stress activation. The prefrontal cortex plays an important role in inhibition of context-dependent stress responses. These regions converge on subcortical structures that relay information to paraventricular nucleus corticotropin-releasing hormone neurons, controlling the magnitude and duration of HPA axis stress responses. The output of these neural networks determines the net effect on glucocorticoid secretion, both within the normal adaptive range and in pathological circumstances.


2021 ◽  
Author(s):  
Suliman Khan ◽  
V Wee Yong ◽  
Mengzhou Xue

Abstract Biological rhythms regulate physiological activities. Shiftwork disrupts normal circadian rhythms and may increase the risk of cancer through unknown mechanisms. To mimic environmental light/dark changes encountered by shift workers, a protocol called “chronic jet lag (CJL)” induced by repeatedly shifting light-dark cycles has been used. Here, we subjected mice to CJL by advancing light–dark cycle by 6 hours every 2 days, and conducted RNA sequencing to analyze the expression profile and molecular signature in the brain areas of prefrontal cortex and nucleus accumbens. We also performed positron emission tomography (PET) imaging to monitor changes related to glucose metabolism in brain. Our results reveal systematic reprogramming of gene expression associated with cancer related pathways and metabolic pathways in prefrontal cortex and nucleus accumbens. PET imaging indicates that glucose uptake level was significantly reduced in whole brain as well as the individual brain regions. Moreover, qPCR analysis describes that the expression levels of cancer related genes were altered in prefrontal cortex and nucleus accumbens. Overall, these results suggest a molecular and metabolic link with CJL mediated cancer risk, and generate hypotheses on how CJL increases the susceptibility to cancer.


2017 ◽  
Author(s):  
Kyle Stanley Burger

OBJECTIVE: Although soft drinks are heavily advertised, widely consumed, and have been associated with obesity, little is understood regarding neural responsivity to soft drink intake, anticipated intake, and advertisements. METHODS: Functional MRI was used to assess examine neural response to carbonated soft drink intake, anticipated intake and advertisement exposure as well as milkshake intake in 27 adolescents that varied on soft drink consumer status.RESULTS: Intake and anticipated intake of carbonated Coke® activated regions implicated in gustatory, oral somatosensory, and reward processing, yet high-fat/sugar milkshake intake elicited greater activation in these regions versus Coke intake. Advertisements highlighting the Coke product vs. non-food control advertisements, but not the Coke logo, activated gustatory and visual brain regions. Habitual Coke consumers vs. non-consumers showed greater posterior cingulate responsivity to Coke logo ads, suggesting that the logo is a conditioned cue. Coke consumers exhibited less ventrolateral prefrontal cortex responsivity during anticipated Coke intake relative to non-consumers. CONCLUSIONS: Results indicate that soft drinks activate reward and gustatory regions, but are less potent in activating these regions than high-fat/sugar beverages, and imply that habitual soft drink intake promotes hyper-responsivity of regions encoding salience/attention toward brand specific cues and hypo-responsivity of inhibitory regions while anticipating intake.


2004 ◽  
Vol 16 (9) ◽  
pp. 1505-1516 ◽  
Author(s):  
Katrien Denys ◽  
Wim Vanduffel ◽  
Denis Fize ◽  
Koen Nelissen ◽  
Hiromasa Sawamura ◽  
...  

The prefrontal cortex supports many cognitive abilities, which humans share to some degree with monkeys. The specialized functions of the prefrontal cortex depend both on the nature of its inputs from other brain regions and on distinctive aspects of local processing. We used functional MRI to compare prefrontal activity between monkey and human subjects when they viewed identical images of objects, either intact or scrambled. Visual object-related activation of the lateral prefrontal cortex was observed in both species, but was stronger in monkeys than in humans, both in magnitude (factors 2–3) and in spatial extent (fivefold or more as a percentage of prefrontal volume). This difference was observed for two different stimulus sets, at two field strengths, and over a range of tasks. These results suggest that there may be more volitional control over visual processing in humans than in monkeys.


Author(s):  
Lee Peyton ◽  
Alfredo Oliveros ◽  
Doo-Sup Choi ◽  
Mi-Hyeon Jang

AbstractPsychiatric illness is a prevalent and highly debilitating disorder, and more than 50% of the general population in both middle- and high-income countries experience at least one psychiatric disorder at some point in their lives. As we continue to learn how pervasive psychiatric episodes are in society, we must acknowledge that psychiatric disorders are not solely relegated to a small group of predisposed individuals but rather occur in significant portions of all societal groups. Several distinct brain regions have been implicated in neuropsychiatric disease. These brain regions include corticolimbic structures, which regulate executive function and decision making (e.g., the prefrontal cortex), as well as striatal subregions known to control motivated behavior under normal and stressful conditions. Importantly, the corticolimbic neural circuitry includes the hippocampus, a critical brain structure that sends projections to both the cortex and striatum to coordinate learning, memory, and mood. In this review, we will discuss past and recent discoveries of how neurobiological processes in the hippocampus and corticolimbic structures work in concert to control executive function, memory, and mood in the context of mental disorders.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiao Lin ◽  
Jiahui Deng ◽  
Kai Yuan ◽  
Qiandong Wang ◽  
Lin Liu ◽  
...  

AbstractThe majority of smokers relapse even after successfully quitting because of the craving to smoking after unexpectedly re-exposed to smoking-related cues. This conditioned craving is mediated by reward memories that are frequently experienced and stubbornly resistant to treatment. Reconsolidation theory posits that well-consolidated memories are destabilized after retrieval, and this process renders memories labile and vulnerable to amnestic intervention. This study tests the retrieval reconsolidation procedure to decrease nicotine craving among people who smoke. In this study, 52 male smokers received a single dose of propranolol (n = 27) or placebo (n = 25) before the reactivation of nicotine-associated memories to impair the reconsolidation process. Craving for smoking and neural activity in response to smoking-related cues served as primary outcomes. Functional magnetic resonance imaging was performed during the memory reconsolidation process. The disruption of reconsolidation by propranolol decreased craving for smoking. Reactivity of the postcentral gyrus in response to smoking-related cues also decreased in the propranolol group after the reconsolidation manipulation. Functional connectivity between the hippocampus and striatum was higher during memory reconsolidation in the propranolol group. Furthermore, the increase in coupling between the hippocampus and striatum positively correlated with the decrease in craving after the reconsolidation manipulation in the propranolol group. Propranolol administration before memory reactivation disrupted the reconsolidation of smoking-related memories in smokers by mediating brain regions that are involved in memory and reward processing. These findings demonstrate the noradrenergic regulation of memory reconsolidation in humans and suggest that adjunct propranolol administration can facilitate the treatment of nicotine dependence. The present study was pre-registered at ClinicalTrials.gov (registration no. ChiCTR1900024412).


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Alexander A. Aabedi ◽  
Sofia Kakaizada ◽  
Jacob S. Young ◽  
Jasleen Kaur ◽  
Olivia Wiese ◽  
...  

AbstractLexical retrieval requires selecting and retrieving the most appropriate word from the lexicon to express a desired concept. Few studies have probed lexical retrieval with tasks other than picture naming, and when non-picture naming lexical retrieval tasks have been applied, both convergent and divergent results emerged. The presence of a single construct for auditory and visual processes of lexical retrieval would influence cognitive rehabilitation strategies for patients with aphasia. In this study, we perform support vector regression lesion-symptom mapping using a brain tumor model to test the hypothesis that brain regions specifically involved in lexical retrieval from visual and auditory stimuli represent overlapping neural systems. We find that principal components analysis of language tasks revealed multicollinearity between picture naming, auditory naming, and a validated measure of word finding, implying the existence of redundant cognitive constructs. Nonparametric, multivariate lesion-symptom mapping across participants was used to model accuracies on each of the four language tasks. Lesions within overlapping clusters of 8,333 voxels and 21,512 voxels in the left lateral prefrontal cortex (PFC) were predictive of impaired picture naming and auditory naming, respectively. These data indicate a convergence of heteromodal lexical retrieval within the PFC.


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